CD8^+T淋巴细胞与高血压心肌纤维化的研究进展  

CD8+ T lymphocytes and myocardial fibrosis in hypertension

作　　者：耿丽[1] 孟晓萍[1] 

机构地区：[1]吉林大学第二医学院,吉林长春130021

出　　处：《现代生物医学进展》2010年第6期1198-1200,共3页Progress in Modern Biomedicine

基　　金：吉林省科技厅项目(200705229)

摘　　要：血管生长因子增多,血管平滑肌细胞增殖和炎症在血管重塑方面起到了关键的作用。这种低级的炎症反应导致粘附分子表达,白细胞的侵入,细胞因子的产生,氧化应激的增加,从而激活免疫细胞和血管炎症信号通路,使T淋巴细胞及巨噬细胞等细胞活化,产生和释放多种活性因子,激活心肌的细胞外基质生成细胞,引起胶原形成及代谢异常,并可导致心肌实质细胞的变性、坏死或亚细胞结构变化等,从而引起心肌纤维化一系列病理生理变化。本文主要就CD8+T淋巴细胞在高血压心肌纤维化炎症反应中的细胞毒性作用、诱导细胞凋亡作用、分泌大量的炎症因子、增加MMPs的活性从而影响心肌纤维化的形成等方面做一综述!The vascular growth and proliferation of vascular smooth muscle cells, inflammation plays a key role in the vascular remodeling that Low-grade inflammation participates in the mechanisms leading to blood pressure （BP） elevation. Increased expression of adhesion molecules and their legends, leukocyte extravasation, cytokine production, increased oxidative stress, activation of immunecells and proinflammatory signaling pathways in arteries from hypertensive patients ,T lymphocytes and macrophages and other cells are activated, produce and release a variety of active factors, activate myocardial extracellular matrix-producing cells, , activate myocardial extracellular matrix-producing cells, cause the collagen formation and metabolic abnormalities, result in the myocardial parenchymal cell egeneration, necrosis or subcellular structural changes etc, cause a series of pathophysiological changes. In this paper, the action of the CD8＋ T lymphocytes in Inflammatory response in myocardial fibrosis, include cytotoxic effect, induced apoptosis, secrete large amounts of inflammatory cytokines, increase the activity of MMPs to affect the formation of myocardial fibrosis etc.be described.

关 键 词：心肌纤维化 CD8+T淋巴细胞 胶原 高血压 

分 类 号：R541.3[医药卫生—心血管疾病]